Implantable medical device for treating cardiac mechanical dysfunction by electrical stimulation

Abstract

The above-described methods and apparatus are believed to be of particular benefit for patients suffering heart failure including cardiac dysfunction, chronic HF, and the like and all variants as described herein and including those known to those of skill in the art to which the invention is directed. It will understood that the present invention offers the possibility of monitoring and therapy of a wide variety of acute and chronic cardiac dysfunctions. The current invention provides systems and methods for delivering therapy for cardiac hemodynamic dysfunction.

Description

[0001] This patent disclosure claims the benefit of provisional U.S. Patent Application Serial No. 60 / 315,316 filed Aug. 28, 2001 the entire contents of which are hereby incorporated by reference herein.[0002] This patent disclosure hereby incorporates by reference commonly assigned U.S. Pat. No. 6,438,408 which issued Aug. 20, 2002 and entitled, "IMPLANTABLE MEDICAL DEVICE FOR MONITORING CONGESTIVE HEART FAILURE," by Lawence J. Mulligan et al. and International Application No. PCT / US01 / 50276 invented by Deno et al. and entitled, "IMPLANTABLE MEDICAL DEVICE FOR TREATING CARDIAC MECHANICAL DYSFUNCTION BY ELECTRICAL STIMULATION."[0003] The present invention relates generally to implantable medical devices and more specifically to monitoring signs of acute or chronic cardiac mechanical dysfunction such as heart failure (HF), cardiogenic shock, pulseless electrical activity (PEA), or electromechanical dissociation (EMD), and providing appropriate therapies.[0004] Patients suffering from...

AI Technical Summary

Benefits of technology

0097] The first change to existing and prior art regimens is to increase the number of shocks beyond the present upper limit.

0098] A second change is to increase the time bet

Problems solved by technology

As the disease progresses, the lack of cardiac output may contribute to the failure of other body organs, leading to cardiogenic shock, arrhythmias, electromechanical dissociation, and death.

Although these agents may be beneficial in specific settings, they require administration of a drug, often by intravenous route, with systemic side effects and the time-consuming involvement of skilled clinicians.

However, the SR continues to take up further calcium with the result that the subsequent cardiac cycle causes a large release of calcium from the SR and the myocyte contracts more vigorously.

However, determining the appropriate pacing parameters is difficult.

As a direct result of a tachycardia or as a sequela, cardiac function may deteriorate to the point of greatly reduced cardiac output and elevated diastolic pressure.

However, prior art systems have not achieved a comprehensive therapy regimen that coordinates these mechanisms in a manner that is both safe and effective.

One problem involves the dangers associated with delivering stimulation during a nonrefractory period to achieve PESP.

A second problem may be a shift in the magnitude of resulting potentiation or refractory interval due to the course of disease or medication.

These may lead to unacceptable levels of potentiation performance, or loss of effect altogether.

Another problem associated with PESP is that the added ventricular depolarization may cause the loss of AV conduction during the next cardiac cycle.

This results in loss of the next intrinsic depolarization in the ventricle.

The resulting pattern may be unstable, characterized by intermittent shifts between 2:1 and 1:1 conduction which may offset the other benefits provided by the PESP since ventricular filling is compromised.

This results in an extra systole that increases contractile function and stroke volume on subsequent contractions.

Institution of PESP therapy may result in intermittent 2:1 AV block.

Unfortunately, 2:1 conduction may produce a ventricular rate that is too slow where as 1:1 conduction with PESP may result in a ventricular rate that is too fast.

When PESP therapy is initiated, a 2:1 AV block typically occurs (and can be depicted with a second waveform "B") although the 2:1 AV block is often unstable.

The use, however, of a mechanical sensor such as a pressure sensor or an accelerometer to determine whether or not to apply therapy has the drawback in that external treatments of PEA/EMD such as cardiac chest compressions may introduce error into the physiologic signals, inhibiting or delaying therapy when it may be needed.

The vulnerable period represents a time period during which an electrical pulse delivered at, or above, a pre-determined amplitude has the risk of causing a VT or VF episode.

Further delays of the stimulation diminish the amount of potentiation.

Stimulation too early (i.e., prematurely) results in no additional potentiation at all since the myocardium is refractory.

However, the inventors have discovered that such a risk is quite low if single PESP pulses are delivered

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